β-Endorphin is present in active and inactive forms in rat gastric antrum

Rosenquist, Grace L.; Maruthainar, K.; Smyth, Derek G.

doi:10.1016/0006-291x(86)90520-6

Cited by 11 publications

(2 citation statements)

References 14 publications

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“…Moreover, (3-EP immunoreactive material has been reported in several other mammalian peripheral tissues such as pancreas, stomach, gonads, adrenal gland, thyroid and lung [ l l , 13, 141. This widespread P-EP immunoreactivity is not fully characterized and the existence of several immunoreactive 6-EP related peptides in plasma is highly possible [15]. It is therefore important to characterize the specificity of a (3-EP RIA applied to measurements in plasma.…”

Section: Discussionmentioning

confidence: 99%

Plasma β-endorphin during clinical and experimental ischaemic pain

Bach

Fahrenkrug

Jensen

et al. 1987

Scand J Clin Lab Invest

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P-endorphin during clinical and experimental ischaemic pain. Scand J Clin Lab Invest 1987; 47: 751-758.An improved radio-immunoassay using an antiserum directed towards the N-terminal part of the endogenous opioid peptide f3-endorphin 1-31 (f3-EP) was validated and applied to a study of P-EP in plasma during ischaemic pain. Experimental ischaemic pain induced in seven healthy volunteers by the submaximal effort tourniquet test did not change plasma P-EP or adrenocorticotrophin. Plasma P-EP was determined in 21 patients with acute myocardial infarction (AMI) and in seven patients with unstable angina pectoris. Plasma P-EP was 4.9 fmoVml with 95% confidence limits, 3.2-7.8 fmol/ml in AM1 patients at admittance, and 2.9 (2.G3.4) fmoUml one week later in stable and pain-free condition (p<0.05). The level in 49 healthy persons was 2.8 (2.4-2.9) fmol/ml. Elevated P-EP levels were found in five AM1 patients with cardiogenic shock and in four AM1 patients dying within 24 h after admittance compared to the rest of AM1 patients (p<0.02). P-EP was not elevated during unstable angina pectoris, although pain scores were similar to AMI. The AM1 group revealed a significant, although weak, positive correlation between plasma P-EP and pain score (Spearman r=0.49. p<0.05), while there was no correlation during unstable angina pectoris. P-EP was not correlated to the amount of morphine required within the 48 h after admittance of AM1 patients. We conclude that the increase of p-EP in plasma during AM1 may be due to stressful factors other than ischaemic pain and that it is questionable whether p-EP in plasma is related to antinociception.The 31 amino acid residue peptide, Panalgetic properties when tested in biological endorphin (P-EP), characterized by potent assays [l], is cleaved from the 31 kDa common 75 1 Scand J Clin Lab Invest Downloaded from informahealthcare.com by McMaster University on 11/18/14 For personal use only. Scand J Clin Lab Invest Downloaded from informahealthcare.com by McMaster University on 11/18/14 For personal use only. Scand J Clin Lab Invest Downloaded from informahealthcare.com by McMaster University on 11/18/14 For personal use only.

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Section: Discussionmentioning

confidence: 99%

Plasma β-endorphin during clinical and experimental ischaemic pain

Bach

Fahrenkrug

Jensen

et al. 1987

Scand J Clin Lab Invest

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“…However, current research has indicated the presence of opioid receptors and an opioid synthesis in several organs in animals [37][38][39]. Endogenous opioids have been shown in numerous studies to be synthetized in and to have effects on the myocardium [2,3,6].…”

Section: Discussionmentioning

confidence: 99%

Myocardial Turnover of Endogenous Opioids and Calcitonin-Gene-Related Peptide in the Human Heart and the Effects of Spinal Cord Stimulation on Pacing-Induced Angina Pectoris

Eliasson¹,

Mannheimer²,

Waagstein³

et al. 1998

Cardiology

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Earlier studies have shown that spinal cord stimulation (SCS) has antianginal and anti-ischemic effects in severe coronary artery disease. In the present study, 14 patients were subjected to right-sided atrial catheterization and atrial pacing. The patients were paced to angina during a control session and during spinal cord stimulation. Myocardial extraction of β-endorphin (BE) during control pacing (8 ± 22%) changed to release at the maximum pacing rate during treatment (–21 ± 47%, a negative value representing release). Furthermore, the results indicate local myocardial turnover of leuenkephalin, BE and calcitonin-gene-related peptide. In addition, it is implied that SCS may induce myocardial release of BE which could explain the beneficial effects in myocardial ischemia.

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Posttranslational Processing of Gut Peptides

Dickinson

Yamada

1989

Comprehensive Physiology

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β-Endorphin is present in active and inactive forms in rat gastric antrum

Cited by 11 publications

References 14 publications

Plasma β-endorphin during clinical and experimental ischaemic pain

Plasma β-endorphin during clinical and experimental ischaemic pain

Myocardial Turnover of Endogenous Opioids and Calcitonin-Gene-Related Peptide in the Human Heart and the Effects of Spinal Cord Stimulation on Pacing-Induced Angina Pectoris

Posttranslational Processing of Gut Peptides

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